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J. Biol. Chem., Vol. 279, Issue 41, 42732-42741, October 8, 2004

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Heparan Sulfate Structure in Mice with Genetically Modified Heparan Sulfate Production^*

Johan Ledin, William Staatz, Jin-Ping Li, Martin Götte¶, Scott Selleck, Lena Kjellén, and Dorothe Spillmann||

From the Department of Medical Biochemistry and Microbiology, University of Uppsala, SE-75123 Uppsala, Sweden, The Developmental Biology Center, Department of Pediatrics and Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, Minnesota 55455, and ^¶Department of Obstetrics and Gynecology, University Hospital, D-48149 Münster, Germany

Using a high throughput heparan sulfate (HS) isolation and characterization protocol, we have analyzed HS structure in several tissues from mice/mouse embryos deficient in HS biosynthesis enzymes (N-deacetylase/N-sulfotransferase (NDST)-1, NDST-2, and C5-epimerase, respectively) and in mice lacking syndecan-1. The results have given us new information regarding HS biosynthesis with implications on the role of HS in embryonic development. Our main conclusions are as follows. 1) The HS content, disaccharide composition, and the overall degree of N- and O-sulfation as well as domain organization are characteristic for each individual mouse tissue. 2) Removal of a key biosynthesis enzyme (NDST-1 or C5-epimerase) results in similar structural alterations in all of the tissues analyzed. 3) Essentially no variation in HS tissue structure is detected when individuals of the same genotype are compared. 4) NDST-2, although generally expressed, does not contribute significantly to tissue-specific HS structures. 5) No change in HS structure could be detected in syndecan-1-deficient mice.

Received for publication, May 14, 2004 , and in revised form, July 12, 2004.

^* This work was supported by the Swedish Research Council (Grants 32X-15023 and 521-2002-3413), the programme "Glycoconjugates in Biological Systems" and Grant A303:156e sponsored by the Swedish Foundation for Strategic Research, Polysackaridforskning AB, Gustaf V:s 80-årsfond, Swedish Cancer Society (4708-B02-01XAA), and the "Forschungsverbund Nordrhein-Westfalen-Schweden" (to M. G.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^|| To whom correspondence should be addressed. Tel.: 46-18-471-4367; Fax: 46-18-471-4209; E-mail dorothe.spillmann{at}imbim.uu.se.

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